Epidemiological studies indicate that behavioral stresses can participate in the development of primary hypertension, but the mediating physiological mechanisms remain to be clarified. Studies from our laboratory have provided support for the view that hypertension can develop as an interaction between high sodium intake and aversive behavioral conditioning procedures that suppress respiratory activity. The mechanism is hypothesized to involve increases in pCO2, renal Na/H exchange, renal Na retention, stimulation of endogenous digitalis-like sodium pump inhibitors (EDLF) and inhibition of Na pump activity in vascular smooth muscle, leading to increases in intravascular Na and Ca, and increased total peripheral resistance in a context of increased plasma volume. During the current year, stability of resting end tidal CO2 (PETCO2) in normotensive human subjects, its associations with personality factors, and the differential effects of high dietary sodium intake on resting and ambulatory blood pressure of younger (below age 40) and older (above age 40) humans as a function of individual resting PETCO2 were investigated. Resting PETCO2 was found to be relatively stable over a six month period, and to be highest in subjects who were high on the NEO Neuroticism Scale (which assesses experience of negative emotional states). High dietary Na intake was associated with increased overnight urinary Na excretion and increased body weight in all subjects, regardless of PETCO2 status. In older adults, higher resting PETCO2 was associated with increases in both resting and 24-hour blood pressure. In younger adults, high Na intake increased 24-hour, but not resting, blood pressure. Plasma EDLF was higher in subjects with higher resting PETCO2, both before and after Na loading, indicating increased plasma volume in Na sensitive subjects. These are the first studies to identify PETCO2 as a risk factor for Na sensitivity, and open a new area of investigation of the origins of individual differences in resting PETCO2.